International Journal of Hygiene and Environmental Health 218 (2015) 111

Contents lists available at ScienceDirect

International Journal of Hygiene and

Environmental Health
journal homepage: www.elsevier.com/locate/ijheh

Review

Effect of long-term outdoor air pollution and noise on cognitive and

psychological functions in adults
Lilian Tzivian a, , Angela Winkler b , Martha Dlugaj b , Tamara Schikowski a,d,e ,
Mohammad Vossoughi a , Kateryna Fuks a , Gudrun Weinmayr a , Barbara Hoffmann a,c
a

IUF-Leibniz Research Institute for Environmental Medicine, Dsseldorf, Germany

Department of Neurology, University Hospital of Essen, University of Duisburg-Essen, Essen, Germany
c
Medical Faculty, Heinrich Heine University of Dsseldorf, Dsseldorf, Germany
d
Swiss Tropical and Public Health Institute, Basel, Switzerland
e
University of Basel, Basel, Switzerland
b

a r t i c l e

i n f o

Article history:
Received 2 June 2014
Received in revised form 20 August 2014
Accepted 26 August 2014
Keywords:
Cognitive function
Depression
Dementia
Air pollution
Noise
Particulate matter

a b s t r a c t
It has been hypothesized that air pollution and ambient noise might impact neurocognitive function. Early
studies mostly investigated the associations of air pollution and ambient noise exposure with cognitive
development in children. More recently, several studies investigating associations with neurocognitive
function, mood disorders, and neurodegenerative disease in adult populations were published, yielding
inconsistent results. The purpose of this review is to summarize the current evidence on air pollution and
noise effects on mental health in adults. We included studies in adult populations (18 years old) published in English language in peer-reviewed journals. Fifteen articles related to long-term effects of air
pollution and eight articles on long-term effects of ambient noise were extracted. Both exposures were
separately shown to be associated with one or several measures of global cognitive function, verbal and
nonverbal learning and memory, activities of daily living, depressive symptoms, elevated anxiety, and
nuisance. No study considered both exposures simultaneously and few studies investigated progression
of neurocognitive decline or psychological factors. The existing evidence generally supports associations
of environmental factors with mental health, but does not sufce for an overall conclusion about the
independent effect of air pollution and noise. There is a need for studies investigating simultaneously air
pollution and noise exposures in association mental health, for longitudinal studies to corroborate ndings from cross-sectional analyses, and for parallel toxicological and epidemiological studies to elucidate
mechanisms and pathways of action.
2014 Elsevier GmbH. All rights reserved.

Introduction
While the associations of air pollution on cardiovascular function and disease have been shown in many studies (Brook et al.,
2010; Rckler et al., 2011), comparatively little is known about
the effect of long-term air pollution on neurocognitive function,
even though sustained neurocognitive function at older age is a
prominent element of healthy ageing and will be one of the main
challenges in our ageing societies. The rst link between ambient

air pollution and neurotoxicity was made by Caldern-Garciduenas

et al. (2002). This work was based on a histological comparison
of brain tissue from dogs, living in high- and low-pollution areas,
respectively. Dogs from highly polluted areas had more damages to

Corresponding author. Tel.: +49 1522 9412016.

E-mail address: Liliana.Tzivian@IUF-Duesseldorf.de (L. Tzivian).
http://dx.doi.org/10.1016/j.ijheh.2014.08.002
1438-4639/ 2014 Elsevier GmbH. All rights reserved.

the bloodbrain barrier, degeneration of cortical neurons, apoptotic

glial white cells, non-neuritic plaques and neurobrillary tangles
compared to dogs from low-polluted areas. Since then, several epidemiological and toxicological studies have investigated chronic
effects of air pollution and ambient noise on neurocognitive function in children and adults.
Most of the epidemiological studies investigated whether the
effect of air pollution was related to the development of cognition during childhood and possible changes of it in adolescence
(Edwards et al., 2010; Freire et al., 2010; Perera et al., 2008;
Siddique et al., 2011). Investigations on the effect of air pollution
on neurocognitive function in adults are still rare. In a recent
review, Guxens and Sunyer (2012) summarized studies on neuropsychological effects of air pollution, including 12 children studies,
and four studies of adult populations of which one concentrated
on short-term air pollution effects. In the most current review
(Block et al., 2012), six studies were related to neurocognitive

L. Tzivian et al. / International Journal of Hygiene and Environmental Health 218 (2015) 111

and psychological functions of adults. These reviews hypothesized

a potential role of air pollution on white matter lesions and
cerebrovascular pathology in adults that can lead to cognitive
changes in adults. A role of PM in cognitive decits and behavior
impairment in children and elderly was also proposed (Block et al.,
2012; Guxens and Sunyer, 2012).
The association of noise with neurocognitive function is even
less investigated. Most studies on association between ambient
noise and neurocognitive functions measured short-term effects
(Elmenhorst et al., 2010; Schapkin et al., 2006) or investigated the
effect on irrelevant speech in adults (Clark and Srqvist, 2012;
Salame and Baddeley, 1982; Smith and Broadbent, 1992). In most
of the studies, occupational and environmental noise was found to
be related to annoyance that can disturb normal human activities
and lead to somatic and psychosomatic health effects (PasschierVermeer and Passchier, 2000).
Knowledge about biological pathways linking air pollution to
neurocognitive impairment is still scarce. Two possible pathways of
how particulate matter PM can affect neurocognitive function were
hypothesized (Genc et al., 2012). Respiratory intake of PM activates pro-inammatory cytokines in human macrophages, thereby
causing an inammatory response and subsequent oxidative stress.
Inammatory compounds can spill over into the systemic circulation and penetrate the bloodbrain barrier (Genc et al., 2012;
Hirano et al., 2003). This leads to different histological abnormalities in the animal brain (Nemmar et al., 2001).
The second pathway is related to direct entry of PM into the nervous system through the olfactory bulb following nasal inhalation.
Pathological changes in the olfactory bulb were observed in early
stages of Alzheimers disease (AD) (Doty, 2008). Ultrane particles
(UFP) were observed in human olfactory bulb periglomerular neu et al.,
rons after exposure to air pollution (Caldern-Garciduenas
2008). While these pathways pertaining to long-term air pollution
exposure are a major research subject, there is a lack of studies
describing possible pathways of long-term ambient noise exposure
affecting neurocognitive functions.
Recently, further epidemiological studies on long-term neurocognitive effects of air pollution and noise were published (Block
and Calderon-Garciduenas, 2009). These studies investigated adult
participants, used multiple cognitive tests and explored associations with various air pollutants and a wide range of ambient
noise levels. As air pollution and ambient noise in many cases
may have common sources, such as trafc, they may have synergistic effects on neurocognitive function. There are no reviews to
date which integrate the studies on both air pollution and noise
effects on neurocognitive function. The purpose of this article is to
review the up-to-date articles investigating effects of air pollution
and ambient noise on different aspects of mental health, namely
neurocognitive function, mood disorders and neurodegenerative
disease in adult populations.

Methods of the search

We performed a literature search of articles relating long-term
ambient air pollution and ambient noise with mental health (cognitive functions, neurocognitive diseases and mood disorders) in
adults using the two major search engines PubMed and Google
Scholar. Long-term exposure was dened as the average exposure during at least one year. Short-term exposures during the
days or hours before outcome assessment were not included.
For this search, the following keywords were used: Alzheimers
disease, anxiety, central nervous system, cognition, cognitive
function, cognitive decline, depression, dementia, mild cognitive
impairment, mood disorders, neurocognitive effect, Parkinsons
disease, peripheral nervous system, vertigo, air pollution, noise,

noise exposure, particulate matter, particul*, ultrane particles,

ne PM, trafc, alone and in combination. The exact search
history is available on request. An additional search was performed based on the references of the retrieved articles meeting
the inclusion criteria. Inclusion criteria for the articles were: (1)
studies related to the effect of air pollution and ambient noise
exposures on mental health; (2) studies related to adult populations (18 years old); (3) epidemiologic studies published
in English language in peer-reviewed journals. We excluded
from this review ecologic studies and studies on short-term
effects.
Results
The literature search was nished in November 2013. In total, 22
articles were retrieved, of which 14 investigated long-term associations of air pollution, and seven investigated long-term associations
of ambient noise exposure on neurocognitive functions, mood disorders and neurodegenerative disease in adults. Additionally, one
study (Persson et al., 2007) considered both, air pollution and noise.
Six of the 22 reviewed studies (Bocquier et al., 2013; Gatto et al.,
2013; Franssen et al., 2013; Loop et al., 2013; Power et al., 2013;
Wellenius et al., 2012) were published within the last 2 years and
therefore were not included in the reviews of Guxens and Sunyer
(2012) and Block et al. (2012); four of them analyzed neurocognitive effects of air pollution, and twothe effects of trafc and
aircraft noise.
Study design and exposures******
Nine studies related to air pollution conducted cross-sectional
analyses, of those six studies were carried out as cross-sectional
analyses in ongoing cohort studies; two studies conducted
casecontrol analysis (Table 1). In three studies (Lim et al., 2012;
Wellenius et al., 2012; Weuve et al., 2012), follow-up examinations
with repeated assessments of cognitive function were performed.
In the study of Lim et al. (2012), three follow-up examinations
were performed, each 3 years apart, but from 560 participants only
187 were examined all the three times during the study period.
In the study by Wellenius et al. (2012), the follow-up examination
was performed approximately 16.8 months after baseline (median
value). In the study by Weuve et al. (2012), a reexamination was
conducted after 4.3 years. Two studies were performed only in
women (Ranft et al., 2009; Weuve et al., 2012) and two were performed on the same study population which included only men
(Power et al., 2011, 2013).
Of eight studies investigating the association of long-term
noise on neurocognitive function or mood disorders, four studies performed cross-sectional analyses, two studies conducted
a casecontrol analysis; and two studies were cohort studies
(Table 2). One of them (Bocquier et al., 2013) had a retroprospective design. One study was performed only in women
(Yoshida and Osada, 1997). In one casecontrol study (Persson et al.,
2007), asthmatic versus non-asthmatic participants were investigated.
Exposure assessment
Long-term air pollution exposure is mostly approximated by
estimating average exposure at the address of residence at the
time of the outcome assessment or during the years of followup (Dockery et al., 1993). The exposure contrasts investigated are,
therefore, the spatial patterns of air pollution concentration which
in the long run tend to be relatively stable due to similar landuse patterns and long-term meteorology (Cesaroni et al., 2012;

L. Tzivian et al. / International Journal of Hygiene and Environmental Health 218 (2015) 111

Table 1
Main characteristics of epidemiological studies exploring the association of long-term air pollution on cognitive and psychological functions in adults, by alphabetical order
of authors.
Authors, year of
publication, country

Type of analysis

Study population N
(age)

Exposure

Principal outcomes/tests

Investigated cognitive and

psychological functions

Caldern-Garciduenas
et al., 2004, Mexico

Caldern-Garciduenas
et al., 2009, Mexico
Chen and Schwartz,
2009, USA

Cross-sectional

N = 19 (51.2 4.9)

PM, O3

Histological examinations

Cross-sectional

N = 87 (21.0 2.6)

PM2.510 , PM2.5

Cross-sectional

N = 1764
(37.4 10.9)

PM10 , O3

Casecontrol

N = 52,986 (not
available)
N = 1496
(60.5 8.1)

NO2 , Ambient Mn

Alzheimer like pathology; COX2

and mRNA levels
University of Pennsylvania smell
identication test (UPSIT)
Simple reaction time test (SRTT),
Symbol-digit substitution test
(SDST), Serial-digit learning test
(SDLT)
l-DOPA prescription; physicians
diagnosis of Parkinson disease (PD)
Boston Naming Test, Symbol digit
modalities test, Trail Making Test
(TMT) A/B, Letter-number
sequencing, Animal naming,
California verbal learning test,
Paragraph recall, Faces, Block
design, Judgment of line
orientation
Korean version of the Geriatric
depression scale-short form
(SGDK-K)
Incidence of cognitive
declineSix-Item Screener
Psychic trait anxiety score

Finkelstein and Jerrett,

2007, Canada
Gatto et al., 2013, USA

Cross-sectional

Lim et al., 2012,

Republic of Korea

Longitudinal
follow-up 3 years

N = 357 (71.0 5.0)

PM10 , CO, SO2 , NO2 ,

O3

Loop et al., 2013, USA

Cross-sectional

PM2.5

Persson et al., 2007,

Sweden

Casecontrol

N = 20,150
(64.0 9.2)
N = 22,693
(43.0 13.0)

Power et al., 2011,

USA

Cross-sectional

N = 680 (71.0 7.0)

NOx, Wood
burning; industrial
smells
BC

Power et al., 2013, USA

Cross-sectional

N = 629 (70.0 7.1)

BC

MMSE, Pattern comparison task,

Digit span backward test,
Long-term verbal IR and DR,
Constructional praxis

Ranft et al., 2009,

Germany

Cross-sectional

N = 399 (74.1 2.6)

PM10

Neuropsychological CERAD-Plus
battery: MMSE, TMT, Stroop
color-word test, long-term verbal
IR and DR, Constructional praxis,
DR of gures

Sun and Gu, 2008,

China

Cross-sectional

N = 7358
(83.6 11.4)

API**

MMSE; Activity of daily living

(ADL); Self-reported health

Wellenius et al., 2012,

USA

Cohort follow-up
(median), 16.8
years

N = 765 (78.1 5.4)

Proximity to
nearest road, BC

MMSE; Hopkins verbal learning

test-revised (HVLT-R); TMT;
Clock-in-the-box test (CIB);
Category and letter uency tests

Weuve et al., 2012, USA

Cohort follow-up
4.3 years

N = 10,409
(74.0 2.2)

PM10 ; PM2.5 ,
Coarse PM

Zeng et al., 2010, China

Cohort follow-up 7
years

N = 15,873 (86.3)

API**

Telephone interview for cognitive

status (TICS); 10-Words DR; East
Boston memory test (EBMT);
Category uency; Digit span
backward test, modied MMSE
ADL; MMSE; cumulative decits
index (DI); telephone interview for
cognitive status, Self-reported
health

*Additionally other environmental factors were measured.

**Air pollution index that includes SO2 , NO2 , PM10 , CO, O3 .

O3 , NO2 , PM2.5

Mini-Mental State Examination

(MMSE), Pattern comparison task,
Digit span backward test,
Long-term verbal immediate recall
(IR) and delayed recall (DR),
Constructional praxis

Olfactory function
Attention and information
processing speed, verbal
memory

Attention, information
processing speed,
confrontation naming,
executive functions, verbal
memory, nonverbal
memory, visuoconstruction

Depressive symptoms

Anxiety

Attention, working
memory, long-term verbal
memory
(immediate/delayed recall,
consolidation and
recognition),
visuoconstruction, global
cognition
Attention, working
memory, long-term verbal
memory,
visuoconstruction, global
cognition
Attention, information
processing speed,
confrontation naming,
executive functions, verbal
memory, nonverbal
memory,
visuoconstruction, global
cognition, depression,
olfactory function
Global cognition,
satisfaction with health,
ability to perform everyday
activities
Global cognition,
long-term verbal memory,
attention and information
processing speed,
executive functions,
cognitive exibility,
divided attention
Global cognition, long term
verbal memory, executive
functions

Global cognition, ability to

perform everyday
activities, satisfaction with
health

L. Tzivian et al. / International Journal of Hygiene and Environmental Health 218 (2015) 111

Table 2
Main characteristics of epidemiological studies exploring the association of ambient noise on cognitive and psychological functions in adults.
Authors, year of publication,
country

Type of analysis

Study population N

Exposures

Principal outcomes/tests

Investigated functions

Bocquier et al., 2013, France

Retro-prospective
longitudinal follow-up
1 year
Qualitativequantitative
casecontrol
Longitudinal follow-up
5 years

N = 190,617
(41.5 12.5)

LAEQ , 22-6h #

Mean number of
anxiolytic-hypnotic purchases

N = 63 (56.4 16.0)

Trafc noise

Migraine; headache; depressive

disorders; anxiety disorders*

Emotional status

N > 8000 (45.2)

Self-reported health*

Satisfaction with
health

Chiovenda et al., 2007, Italy

Cross-sectional

N = 81 (42.2 7.7)

Road trafc;
railway; aircraft
noise
Noise level for
8 h/day

Franssen et al., 2013, Netherlands

Cross-sectional

N = 11,812 (>18.0)

Digit span forward WAIS-R;

attentive matrices; Digit span
backward; arithmetic reasoning;
Raven PM38; Stroop color-word
test; State-trait anxiety
inventory; prole of mood
states*
Self-reported health
questionnaire (VOEG)*
Generalized anxiety disorder
(GAD); anxiety disorder not
otherwise specied (NOS); major
depressive disorder; depressive
disorder NOS; eating disorder
Psychic Trait Anxiety score *

Attention and
information
processing, executive
functions, working
memory, inhibition,
verbal memory,
emotional status
Satisfaction with
health
Emotional status

General nuisance, interference

with daily activities,
psychological symptoms*

Satisfaction with
health

Brand et al., 2009, Switzerland

Brink, 2011, Switzerland

LDEN ## ; LAEQ , 23-7

#
; LAEQ , 22-23 h #
Aircraft noise

Hardoy et al., 2005, Italy

Cross-sectional

N = 355 (1875)

Persson et al., 2007, Sweden

Casecontrol

N = 22,693
(43.0 13.0)

Yoshida and Osada, 1997, Japan

Cross-sectional

N = 366 (20.0-60.0)

LDEN ## , sound from

neighbors; trafc
noise; ventilation
LDEN ##

Emotional status

*Restricted to psychological outcomes.

#
LAEQ equivalent sounds levels calculated over the corresponding time period.
##
LDEN day, evening, night equivalent sound level over 24 h.

Wang et al., 2013). In most studies, the individual residential history of participants before the outcome assessment is not taken
into account. Four studies exploited contrasts between cities: two
et al., 2004, 2009) compared indistudies (Caldern-Garciduenas
viduals from highly polluted cities with those from communities
in low-pollution areas. The two other studies (Sun and Gu, 2008;
Zeng et al., 2010) compared participants living in the cities with
low, medium and high gross domestic products, using citywide
air pollution indices obtained from the Chinese Natural Resources
Database.
Eleven studies exploited within-city exposure contrasts using
different techniques, alone or in combination. Four studies assigned
measured concentrations from the nearest monitoring site (Chen
and Schwartz, 2009; Lim et al., 2012; Loop et al., 2013; Ranft et al.,
2009), three studies interpolated residential exposure from monitoring stations using GIS-based techniques (Gatto et al., 2013;
Persson et al., 2007; Weuve et al., 2012), ve studies used landuse regression models to estimate small-scale spatial contrasts
of residential exposure (Finkelstein and Jerrett, 2007; Wellenius
et al., 2012; Power et al., 2011, 2013; Ranft et al., 2009) and three
studies used trafc indicators such as proximity to the nearest
road or proximity to high trafc as markers of long-term exposure to trafc-related air pollution (Finkelstein and Jerrett, 2007;
Wellenius et al., 2012, Ranft et al., 2009).
Particulate matter less than 2.5 m in diameter (PM2.5 ), particulate matter less than 10 m in diameter (PM10 ) and ozone (O3 ) were
most frequently investigated in the reviewed studieseach one of
them was presented in four different studies. One study (Persson
et al., 2007) investigated exhaust fumes, wood burning and smell
from industrial production without specifying the PM fractions. In
the studies of Sun and Gu (2008) and Zeng et al. (2010), an air
pollution index (API) assessing combined concentrations of sulfur
dioxide (SO2 ), nitrogen dioxide (NO2 ), PM10 , carbon monoxide (CO)
and O3 was used.

Ambient chronic noise is the sound generated by environmental

sources (Passchier-Vermeer and Passchier, 2000). Road trafc was
the most commonly investigated environmental source of noise.
Seven of the eight studies investigated road trafc noise and two
studies (Franssen et al., 2013; Hardoy et al., 2005) investigated aircraft noise. In one study (Franssen et al., 2013), the additional noise
from neighborhood and from ventilation systems was assessed.
Trafc noise assessment was performed using dedicated environmental noise prediction models (Bocquier et al., 2013; Persson
et al., 2007, Yoshida and Osada, 1997), direct measurements (Brand
et al., 2009), mandatory noise mapping available through ofcial
databases (Brink, 2011; Chiovenda et al., 2007), or by the use of
surrogate markers such as occupation. Most commonly, the noise
exposure metrics dayeveningnight noise level, dened as the
equivalent sound level over 24 hLDEN (Leq(24 h) ), or the noise level
during the night period (226 h)LNIGHT were used. In three studies, noise levels were stratied for analysis to groups of 5 dB(A)
(Bocquier et al., 2013; Brink, 2011; Yoshida and Osada, 1997). In one
study (Chiovenda et al., 2007), high road trafc noise exposed police
ofcers were compared to low noise exposed ofce employees. Aircraft noise exposure for two cross-sectional studies (Franssen et al.,
2013; Hardoy et al., 2005) was assessed by proximity of residential
addressed to the nearest airport, and additionally stratied into categories of 5 dB(A), derived from the National Aerospace Laboratory
mathematical noise model (Franssen et al., 2013).
Outcome assessment
In most of the studies related to air pollution, neuropsychological tests investigating the impairment of different cognitive
domains, such as working memory, verbal memory or executive
functions, were used. Studies investigating the association of longterm noise exposure with the central nervous system functions
mostly used different assessment methods than studies on air

L. Tzivian et al. / International Journal of Hygiene and Environmental Health 218 (2015) 111

pollution. Only two cognitive tests (Digit span test and Stroop
color-word test) were used both in air pollution and noise studies, making direct comparisons between air pollution and noise
effects difcult. Few studies investigated mood disorders, clinical
diagnosis of disease, medication intake or pathological ndings.
Most studies used comprehensive, but unspecic tests with low
sensitivity to assess global cognitive function. In seven studies, the
Mini-Mental State Examination (MMSE) was used (Power et al.,
2011, 2013; Ranft et al., 2009; Sun and Gu, 2008; Wellenius et al.,
2012; Weuve et al., 2012; Zeng et al., 2010), which consists of a
30-item self-administered questionnaire, and which can also be
assessed with a telephone interview. One study applied the SixItem Screener to assess global cognitive function (Loop et al., 2013).
In this test, three items have to be recalled, and additionally the
orientation to year, month and day of the week was checked.
Among more specic test of neurocognitive domains, attention and information processing speed was investigated most
frequently. Several studies used the Trail Making Test A (Gatto et al.,
2013; Ranft et al., 2009; Wellenius et al., 2012), in which a number
of targets have to be connected in the correct order. The number of
correctly performed connections during certain time was a marker
of attention and psychomotor speed. Other studies applied a test on
pattern comparison (Power et al., 2011, 2013), a symbol-digit substitution test (Chen and Schwartz, 2009), a simple reaction time
test (Chen and Schwartz, 2009) and a complex attention test like
the symbol digit modalities test (Gatto et al., 2013) to check the
attention and memory of participants. An additional test that was
used to check participants attentive capacity in studies of noise
effects is the attentive matrices test (Chiovenda et al., 2007); this
test assessed information processing as well.
Another frequently tested domain of cognitive function is verbal memory. It was in most cases assessed using word lists (1016
words) that were presented once or several times to the participant (Gatto et al., 2013; Power et al., 2011, 2013; Ranft et al., 2009;
Wellenius et al., 2012; Weuve et al., 2012). After every learning
trial, the number of immediately recalled words serves as measure
of verbal memory. After a delay and/or an additional interference
list, the participants were asked to recall the previously learned
words (delayed recall). Furthermore, most researchers included a
recognition trial at the end of the test in which a list of words was
shown to the participants, and asked which ones were on the previously learned list. One study (Gatto et al., 2013) examined memory
for verbal information that exceeds the immediate memory span
and needs the contribution of meaning to retention and recall by
using a story recall test. In this study comprehension was examined using recall questions and multiple-choice questions. In the
study of Chen and Schwartz (2009), short-term verbal memory was
assessed with a serial-digit learning test by reproducing a sequence
of eight numbers.
Some studies additionally examined the memory performance
for nonverbal material like previously drafted gures (Ranft et al.,
2009) and faces (Gatto et al., 2013). Faces immediate and delayed
recall test consisted of 16 colored pictures of faces together with
common rst and family name were presented. Later recognition
of the faces was checked using 12 faces from 16 that were presented, and additional 12 distracted faces. The amount of correctly
recognized faces was a marker of visual episodic memory of participants.
The examination of executive function was another main
outcome in many studies, assessed with various specic tests. Cognitive exibility and divided attention were measured using the
Trail Making Test B (Gatto et al., 2013; Ranft et al., 2009; Wellenius
et al., 2012). In this test, a number of targets need to be connected
in order with numerous letter targets on alternating sequence. The
number of correctly performed connections measured cognitive
exibility and divided attention of participants. Verbal uency was

assessed using a semantic category test in which a high number

of items generated for the same category (for instance, animals)
indicated a better performance (Gatto et al., 2013; Wellenius et al.,
2012; Weuve et al., 2012). Similarly, verbal uency was checked
using a phonematic category test (Wellenius et al., 2012). In this
test, the number of words beginning with a given letter served as
measure of phonematic uency. Moreover, working memory was
assessed with the digit span backwards (Power et al., 2011, 2013;
Weuve et al., 2012), a letternumber sequencing task (Gatto et al.,
2013) and the Clock-in-the-Box test (Wellenius et al., 2012). In the
latter case, not only examining working memory, but also planning, organization and visuoconstruction were tested. Inhibition
was assessed with the Stroop color-word test (Ranft et al., 2009). In
this test, the name of a color (e.g., blue, green or red) is printed
in a color not denoted by the name (e.g., the word red printed in
blue ink instead of red ink), and a reaction time to name a color is
measured. An additional outcome used in studies of noise effects
was arithmetic reasoning (Chiovenda et al., 2007).
The cognitive domain of visual construction was also assessed
in several studies (Gatto et al., 2013; Ranft et al., 2009; Power et al.,
2011, 2013) using the Judgment of Line Orientation task, block
design or gure drawing (constructional praxis).
Several studies used clinical diagnoses or pathological ndings
to assess nervous system effects of air pollution. A physicians
diagnosis of Parkinsons disease (PD) and related medication
prescription was investigated in Finkelstein and Jerrett (2007).
et al. (2004) investigated postmortem brain
Caldern-Garciduenas
inammation and Alzheimer like pathology in autopsy brain samples. Among others, cyclooxygenase-2 (COX2) expression and the
42-amino acid form of -amyloid (A42) were examined. In an
et al. (2009),
additional study performed by Caldern-Garciduenas
the olfactory functions using University of Pennsylvania Smell
Identication Test (UPSIT) test were investigated as a marker of
possibility of AD. This test includes self-administrated standardized 40-items, of which 10 items strongly predict conversion to AD
in mild cognitive impairment (MCI) patients.
A few studies also investigated mood disorders, either as
additional outcomes or to statistically control for psychological
disturbances in the air pollution-neurocognitive function analysis. Depression was assessed in two studies (Lim et al., 2012; Ranft
et al., 2009). It was identied by application of the Center of Epidemiological Studies Depression Scale (Ranft et al., 2009) or of the
Geriatric Depression Scale-Short Form (SGDS-K) (Lim et al., 2012),
which includes questions about general life attitude, satisfaction
and activity. Anxiety was investigated in the study of Persson et al.
(2007) using the Swedish Universities Scales of Personality score
(Gustavsson et al., 2000) that summarizes positive answers to seven
anxiety-related statements.
In contrast to air pollution studies, most noise studies examined anxiety and depression (Bocquier et al., 2013; Chiovenda et al.,
2007; Hardoy et al., 2005; Persson et al., 2007; Yoshida and Osada,
1997). Mean number of anxiolytic-hypnotic purchases (Bocquier
et al., 2013), the State-Trait Anxiety Inventory and the Prole of
Mood State (Chiovenda et al., 2007) were assessed in noise studies
only.
Activity of daily living and instrumental activities of daily living
were checked in two air pollution studies (Sun and Gu, 2008; Zeng
et al., 2010). These self-reported activities included personal-care
factors, or outdoor possibilities. For these instruments, participants
having at least one activity limitation were dened as disabled,
in contrast to persons without any disabilities. In these Chinese
studies, additionally self-reported health, as a number of physical complaints (e.g. back pain) and symptoms (e.g. tiredness), was
examined. Self-reported health was also investigated in two noise
studies (Brink, 2011; Franssen et al., 2013), and activity of daily
living in one study (Yoshida and Osada, 1997).

L. Tzivian et al. / International Journal of Hygiene and Environmental Health 218 (2015) 111

Reported associations
The reviewed studies reported their results in a very heterogeneous way (Table 3). Even if the same instruments were used, the
results were generally not presented in a way that allows direct
comparison between studies. This prohibits a systematic metaanalysis of results.
Association with air pollution
In 10 studies, the effect of ambient air pollution on cognitive performance was investigated. In the earliest studies, global cognitive
performance tests were used. In the rst study on global cognitive
performance conducted in 7358 Chinese adults from the Chinese
Longitudinal Health Longevity Survey (CLHLS) (Sun and Gu, 2008),
a positive cross-sectional association of the citywide air pollution
index (API) with reduced MMSE was found. These results were
supported by a consecutive longitudinal analysis in a larger subpopulation of 15,873 participants from the same CLHLS population
(Zeng et al., 2010), using similar methods both for exposure and for
outcome assessment. A one unit increase in API in this study was
associated with a 0.9% increase in odds for MMSE score less than
18 determined as cognitive impairment.
Similar results were obtained for the association of particulate
matter with cognitive functions in the cross-sectional Reasons for
Geographic and Racial Differences in Stroke (REGARDS) study of
20,150 adults in USA (Loop et al., 2013), where a signicant effect
of PM2.5 on incidence of cognitive decline was observed for urban
and mixed (urbanrural) areas, but not for rural areas. These results
were supported by the longitudinal analysis of the Nurses Health
Study Cognitive Cohort (Weuve et al., 2012), in which an association of higher levels of PM2.5-10 and of PM2.5 , with global cognitive
decline was found in 10,409 women over a follow-up period of
4.3 years. Global cognitive decline was signicantly bigger in the
highest versus lowest quintile of exposure.
Inconsistent results were found in studies investigating the
effect of particulate matter on specic cognitive domains. PM2.5
was associated with lower verbal learning in the cross-sectional
analysis of the Women Isoavone Soy Health Trial (WISH) and Early
versus Late Intervention trial With Estradiol (ELITE) study of 1499
US American adults (Gatto et al., 2013). In contrast, increased PM10
levels were not associated with reduced attention and information processing speed and verbal memory after adjustment for race
and socio-economic status (SES) in the cross-sectional study of the
National Health and Nutrition Examination Survey study of 1764
USA residents (Chen and Schwartz, 2009).
Associations of gaseous pollutants with cognitive function also
showed inconsistent results. Although in the cross-sectional study
of Gatto et al. (2013), O3 and NO2 were not associated with global
cognitive function, they were associated with the functions of specic cognitive domains. In this study at high O3 levels (49 ppb),
increasing ozone concentration was associated with lower executive function, while at the intermediate level (3449 ppb) it was
associated with higher logical memory. Exposure to ambient NO2
was associated with lower logical memory (Gatto et al., 2013). In
another cross-sectional study (Chen and Schwartz, 2009), longterm exposure to high levels of O3 was associated with a lower
attention and information processing speed and verbal memory,
even after adjustment for age, sex, gender, SES, life-style and
health covariates. Differences in tests applied for cognitive function assessment in these two studies can be a possible reason for
such inconsistent results.
Associations of other trafc-related exposures with global cognitive function were investigated in four studies, using proximity
to the nearest road and concentration of BC as exposures. All these
studies showed similar results. In two cross-sectional studies of
Power et al. (2011, 2013) performed on Normative Aging Study

(NAS) cohort participants, an adverse association between BC concentration and global cognitive function assessed by MMSE test
was found. This adverse effect of BC on cognitive function was
found predominantly in overweight and obese individuals (p of
interaction = 0.1) and in ever smokers (p for interaction = 0.07).
However, no evidence for effect modication by diabetes, hypertension, smoking or body-mass index (BMI) on the MMSE score was
seen. In the MOBILIZE Boston Study of 765 participants (Wellenius
et al., 2012), an increase in BC level was also associated with lower
MMSE scores and worse performance of additional specic cognitive tests. Proximity to major road was associated with a lower
MMSE, but affected only a part of the other cognitive tests in participants with at least college education and those younger than 77
years. Trafc exposure was associated with reduced performance
in cognitive tests as well in the study of Ranft et al. (2009) that
was performed on 399 Germany women, a part of the Study of
the Inuence of air pollution on Lung function, Inammation and
Aging (SALIA) cohort. In this study, the association was not present
in women older than 74 years, which corresponds to the study of
Wellenius et al. (2012).
The association of air pollution with two neurodegenerative
diseasesAD and PDwas investigated in three studies. Two stud
et al. (2004, 2009) indicated more
ies of Caldern-Garciduenas
Alzheimers-related changes in individuals with higher exposure to
air pollution (reduced olfactory functions, increased COX2 expression and accumulation of A42). Finkelstein and Jerrett (2007)
found an association with prevalence of PD only for an increased
concentration of ambient manganese (Mn), but not for NO2 concentrations.
Associations of air pollution with mood disordersanxiety and
depression, and with activities of daily livingwere investigated
in four studies. In the casecontrol study of Persson et al. (2007)
comparing 22,693 asthmatic and non-asthmatic participants, a signicant association of exhaust fumes from trafc approximated by
NOx concentrations with anxiety was found. In a cross-sectional
study, Sun and Gu (2008) found that API was associated with difculties in coping with personal care activities (bathing, dressing,
eating) and instrumental activities (cooking, shopping, washing
clothes). This study also showed poor self-reported health to be
associated with an increase in air pollution index. These results
were supported by the longitudinal study of Zeng et al. (2010), linking the API with poor self-reported health and increased difculties
in activity of daily living at 4.3 years over a follow-up period (Zeng
et al., 2010). However, in the study of Sun and Gu (2008), the associations of API with activity of daily living were found only for the
cities with high gross domestic product (GDP), and not found for
those with low GDP. An association with depression was investigated in the longitudinal study in 357 inhabitants of Republic
of Korea (Lim et al., 2012). Increased levels of PM10 , O3 and NO2
were found to increase the emotional symptoms of depression, and
PM10 additionally increased the somatic and affective symptoms.
The association with O3 was stronger in participants with a history
of hyperlipidemia than among those without, and little differences
were found between participants with and without cardiovascular
disease (CVD) or myocardial infarction (Lim et al., 2012).
Association with noise
Only one study investigated the association of noise with cognitive functions in 81 police ofcers from high trafc areas and ofce
worker (Chiovenda et al., 2007). A signicant effect of noise was
found for arithmetic reasoning, difculties in logical reasoning and
the Stroop color-word test adjusting for gender, age and education
level.
Associations of noise with health status were investigated in
three studies, reporting inconsistent results (Brink, 2011; Franssen
et al., 2013; Yoshida and Osada, 1997). In the earliest cross-sectional

L. Tzivian et al. / International Journal of Hygiene and Environmental Health 218 (2015) 111
Table 3
Results of studies on long-term air pollution and noise effect on cognitive and psychological functions in adults, by outcome.
Authors, year of publication

Covariates

Obtained results*

Effect of air pollution

Neurocognitive assessment
Cognitive functions
Sun and Gu, 2008

P, L, E

Chen and Schwartz, 2009

P, L, H

Ranft et al., 2009

P, L, H, E

Zeng et al., 2010

Power et al., 2011
Wellenius et al., 2012

P, L
P, L, H

Weuve et al., 2012

P, L

Gatto et al., 2013

P, L

Loop et al., 2013

P, L, H, E

Power et al., 2013

P, L, H

1 unit air pollution index (API): For high gross domestic product (GDP): MMSE score = 2.67,
p < 0.001. For medium GDP: MMSE score = 1.84, p < 0.001
Increased PM10 : SDLT =0.48, 95% CI 0.270.68; SDST = 0.10, 95% CI 0.050.15. After adjustment
for race and SESnon-signicant effect. Increased O3 : SDST = 0.11, 95% CI 0.010.22; SDLT
= 0.52, 95% CI 0.031.01
Trafc exposure: CERAD-plus battery b = 3.8, p < 0.1; Stroop test b = 5.1, p < 0.01; Snifng test
b = 1.3, p < 0.05 (age 74). No independent effect of PM10
1 unit API: cognitive impairment OR = 1.009, p < 0.05
BC (doubling concentration, g/m3 ): MMSE OR = 1.3, 95% CI 1.11.6
100 m from major road: MMSE < 26 for at least college education OR = 1.54, 95% CI 1.102.17; for
77 years OR = 1.34, 95% CI 1.011.76. Not associated with HVLT-R recognition, TMT Part A ad CIB.
Interquartile increase in BC (0.11 g/m3 ): MMSE < 26, OR = 1.15, p = 0.06; worse performance of
HVLT = R immediate recall, p = 0.046
PM2.510 : worse global cognitive score (p for trend 0.01); worse for highest vs. lowest level
(p = 0.003). Highest vs. lowest quintile of PM2.5 : changes in global cognitive score for women
(p = 0.03). Global cognitive score (SD/2 years) per 10 g/m3 increment: PM2.510 0.020 (95% CI
0.32 to 0.008); PM2.5 : 0.018 (95% CI 0.035 to 0.002)
None association with global cognition. Per 10 g/m3 PM2.5 : lower verbal learning ( = 0.32,
p = 0.05). NO2 > 20 ppb: lower logical memory ( = 0.62, p = 0.095). O3 > 49 ppb: lower executive
function ( = 0.66, p = 0.059). O3 range 3449 ppb: higher logical memorywomen ( = 0.46, 95%
CI 0.090.83), adults 60 y. o. ( = 0.51, 95% CI 0.110.91)
Per 10 g/m3 PM2.5 : for urban areaincident cognitive impairment OR = 1.40 (95% CI 1.061.85);
for mixed areasincident cognitive impairment (OR = 0.32, 95% CI 0.110.98). No associations for
rural area and total population
BC (doubling concentration, g/m3 ): for lacked an HFE C282Y low MMSE (OR = 1.37, 95% CI
1.081.73); for at least one HFE H63D variant (OR = 1.74, 95% CI 1.06, 2.87). HFE C282 modies the
association between BC and global cognitive function

Neurodegenerative diseases
Alzheimers disease
et al., 2004
Caldern-Garciduenas

et al., 2009
Caldern-Garciduenas

Parkinson disease (PD)

Finkelstein and Jerrett, 2007

10 g/m3 increases in Mn: PD or Dopa prescription for men OR = 1.041, 95% CI 0.9971.09; for
female: OR = 1.035, 95% CI 0.971.10. With type of clinic as confounder OR = 1.044 (95% CI
1.001.09)

P, H

Exhaust form trafc: anxiety OR = 1.66, p = 0.001

P, K, E

1 unit API: For high GDP: difculties in ADL ( = 1.41, p < 0.01); instrumental ADL ( = 0.98,
p < 0.001), self-related health (OR = 2.20, p < 0.001). For medium GDP instrumental ADL = 0.6,
p < 0.001, self-related health, (OR = 1.87, p < 0.001), no associations with ADL
1 unit API: increased ADL disability (25%, p < 0.001); increased health decits (8%, p < 0.05)

Activity of daily living and mood disorders

Anxiety
Persson et al., 2007
Activity of daily living
Sun and Gu, 2008

Zeng et al., 2010

Depression
Lim et al., 2012

Effect of noise
Neurocognitive assessment
Cognitive functions
Chiovenda et al., 2007

Activity of daily living and mood disorders

Activity of daily living
Yoshida and Osada, 1997
Anxiety
Hardoy et al., 2005
Persson et al., 2007

General nuisance
Yoshida and Osada, 1997
Brand et al., 2009
Depression
Yoshida and Osada, 1997
Hardoy et al., 2005

P, L

Frontal cortex tissue: Elevation of COX2 mRNA in high-exposure group (p = 0.009); elevation of
COX2 immunoreactivity (p = 0.01). Hippocampus tissue: Elevation in COX2 mRNA in high-exposure
group (p = 0.045); no differences in COX2 immunoreactivity between high and low-exposure
groups (p = 0.37)
Mean UPSIT scores lower for high-exposure group (p = 0.03). No differences in UPSIT scores in
different APOE statuses (p = 0.52)

P, L, H

Interquartile increase of PM10 : Increase in composite score of emotional symptoms: 38.2%, p < 0.01,
NO2 118.2%, p < 0.05. Increase in somatic symptoms score 38.9%, p < 0.05. Increase in affective
symptoms score 11.5%, p < 0.01. O3 : Increase in composite score of emotional symptoms 132.5%,
p < 0.05

Differences between police ofcers from high trafc areas and ofce workers: Raven PM38
(t = 3.24, p = 0.002); arithmetic reasoning (t = 2.30, p = 0.024), Stroop color-word test (t = 2.02,
p = 0.047)

Noise 70 dB(A): appetite loss (OR = 5.2***)

General anxiety disorder OR = 2.0 (95% CI 1.04.2); Anxiety disorder NOS OR = 2.9 (95% CI 1.04.1)
Associated with anxiety: trafc noise 55 dB(A), OR = 1.32, p = 0.009; sound from neighbors
OR = 1.47, p = 0.001; trafc vibration OR = 1.37, p = 0.042; sound (other) OR = 1.72, p = 0.003. Sound
from ventilation not associated with anxiety

Noise 70 dB(A): OR = 5.2***

Difference between groups with different noxious environment (X2 = 34.0, p < 0.001)**

Noise 70 dB(A): OR = 2.9***

Major depressive disorder and depressive disorder NOSnot related to aircraft noise

L. Tzivian et al. / International Journal of Hygiene and Environmental Health 218 (2015) 111

Table 3 (Continued)
Authors, year of publication

Covariates

Obtained results*

Bocquier et al., 2013

P, H

Censors blockneighborhood environment: low deprivation, intermediate deprivation, high

deprivation. Regardless deprivation: RR = 1.33 (95% CI 1.021.24) for LAEQ , 22-6 h # 55 dB(A). For
LAEQ , 22-6 h # 55 dB(A) in low deprivation level RR = 1.16 (95% CI 1.011.32) (reference LAEQ , 22-6 h #
<45 dB(A)). For intermediate and high deprivation and for other noise levels (4550 and
5055 dB(A)) in all deprivationsnon-signicant effect

Health status and satisfaction with health

Yoshida and Osada, 1997
Brink, 2011
Franssen et al., 2013

P
P, L
P, L

Noise 70 dB(A): headache OR = 3.0***. No associations with listlessness

No associations in adjusted model
Health indicators not related to noise exposure during the night. Noise 60 dB(A): poor
self-related health OR = 1.61, (95% CI 1.012.56). LDEN ## : headache (OR = 1.16, 95% CI 1.011.34),
tiredness (OR = 1.47, 95% CI 1.261.70), listlessness (OR = 1.17, 95% CI 1.011.36), not fully rested in
the morning (OR = 1.20, 95% CI 1.031.41). Remaining seven complainsnon-signicant

Ppersonal factors, including age, sex, socio-economic status (SES), occupation, marital status, ethnicity, childhood SES, education level, marital status, number of surviving
children, country of origin number of living children. Llifestyle factors, including smoking, drinking, exercise, leisure activities, dark sh consumption, computer experience,
BMI. Hhealth-related factors, including number of consultations with general physician, asthma, diabetes, incident stroke, presence of depressive symptoms, dyslipidemia,
hypertension, blood pressure, triglycerides, HDL. Eenvironmental factors, including indoor air pollution, temperature, season.
*Results related to effect of air pollution/noise only.
**Results are related to all performed measurements, not only to shown in the table.
***Condence intervals are not shown.
#
LAEQ equivalent sounds levels calculated over the corresponding time period.
##
LDEN day, evening, night equivalent sound level over 24 h.

study performed in Japan by Yoshida and Osada (1997) on 366

women, an association of noise 70 dB(A) with self-reported health
status, adjusted for age, duration of residence, type and age of the
house was found for headache, but not for listlessness. However,
only effect estimates without condence intervals were shown,
inhibiting an appraisal of precision of estimation. In the longitudinal study of Brink (2011) with more than 8000 participants and 5
years of follow-up, no signicant association in fully adjusted models was found, while in the unadjusted model daynight level of
road noise LDEN were associated with self-reported general health
status and satisfaction with health. In the cross-sectional study of
Frassen et al. (2013), that investigated self-reported general health
status and intake use of sleep medication in participants living
within a radius of 25 km around the airport, a negative association
was observed only for aircraft noise with health status measures,
and LDEN 60 dB(A) was negatively associated with self-related
health. High LDEN was also signicantly associated with headache
and tiredness in models adjusted for personal confounders and
degree of urbanization. This differs from the study of Yoshida and
Osada (1997) which did not nd such an effect of aircraft noise.
Three studies investigated associations of noise with depression (Yoshida and Osada, 1997; Bocquier et al., 2013; Hardoy et al.,
2005). Yoshida and Osada (1997) showed that depression was associated with noise levels >70 dB(A), with the noise level of 70 dB(A)
being a critical threshold. Bocquier et al. (2013) found in a cohort of
190,617 French that the effect of trafc noise on purchase of antidepressive drugs was only positive in participants living in areas
of low socioeconomic deprivation, while for participants living in
intermediate and high deprivation areas such an effect was nonsignicant. In contrast to these studies, two forms of depressive
disordersmajor depressive disorder and depressive disorder not
otherwise speciedwere not found to be related to aircraft noise
in the cross-sectional study of Hardoy et al. (2005). In this study,
the effect of aircraft noise was investigated in people living in the
vicinity of Elmas airport in contrast to a sample of people living in
cities or rural or mining villages of Italy.
While Hardoy did not nd associations of noise with depression, anxiety disorders were found to be associated with aircraft
noise (Hardoy et al., 2005). No multiple models were constructed
and no accurate noise levels were specied in this study, which
inhibits a comparison with other mentioned studies. Association
between aircraft noise and anxiety disorders were also investigated in a casecontrol study of Persson et al. (2007) that found
no signicant effect of aircraft noise on the trait anxiety (p = 0.101),

however road trafc noise, sounds from neighbors, trafc vibration and sound from other sources were shown to be signicantly
associated with anxiety. Sound from ventilation systems was not
associated with anxiety.
Associations with air pollution and noise
Studies investigating the concurrent effects of air pollution and
noise on neurocognitive outcomes in the same population are
scarce. Only one of the reviewed studies investigated the association of both air pollution and trafc noise (Persson et al., 2007)
with different aspects of mental health in the same study. The
associations were calculated for each one of the exposures (air pollution, noise) separately. However, possible synergistic relations or
interactions between these two exposures were not investigated.
Dis cussion
In this review, we analyzed 22 studies published until November
2013 and summarized the effect of environmental exposures on
different aspects of mental health, namely neurocognitive function, mood disorders and neurodegenerative disease. This review
expands the works of Guxens and Sunyer (2012) and Block et al.
(2012), and supports a possible role of air pollutants on neurocognitive function in the adult population and a role of long-term noise
exposure on mood disorders. However, no evidence is available so
far to disentangle the effects of these two closely related exposures
and outcomes. In this review, we add newly published studies and
expand the investigated outcomes.
All presented studies, assessing the association of air pollution
and noise with neurocognitive functions, found an association at
least for one of the investigated pollutants. However, these associations differed in effect size (Gatto et al., 2013; Loop et al., 2013) and
in the cognitive domain that showed positive associations (Gatto
et al., 2013) and are therefore not easily comparable. Additionally,
in air pollution studies, an association with AD- and PD-related outcomes was observed for highly exposed participants. A positive
association of air pollution and noise was also found for anxiety,
depression and impaired activities of daily living. Associations of
air pollution and noise with mental health outcomes overlapped
little, mostly due to a lack of common outcomes to both types of
exposures studied.
Different associations of air pollution and noise with aspects of
mental health can also be a result of different biological pathways.
Till now, the biological pathways of an effect of long-term air

L. Tzivian et al. / International Journal of Hygiene and Environmental Health 218 (2015) 111

pollution or noise exposure on the brain are not completely

claried. Two different biological pathways were proposed for
long-term effects of air pollution. First, the direct respiratory intake
of air pollutants can provoke a local inammatory effect that leads
to production of pro-inammatory cytokines which can pass into
the systemic circulation and can disrupt the bloodbrain barrier
and damage brain cells (Genc et al., 2012). This pathway was
shown in toxicological studies. For instance, rats exposed to high
levels of diesel exhaust showed elevated levels of interleukin IL-1
expression and elevated levels of tumor-necrosis factor TNF in
brain microglia (Levesque et al., 2011). Secondly, air pollution
et al., 2004;
may affect olfactory functions (Caldern-Garciduenas
Ranft et al., 2009), similar to that found in animal models. Dogs
that were highly exposed to air pollution showed a signicant
increase in DNA damage in olfactory bulbs, the frontal cortex and
et al., 2002).
the hippocampus (Caldern-Garciduenas
Possible associations between noise and neurocognitive function have not been investigated in epidemiological studies so far.
However, experimental studies showed similar effects of air pollution and noise on animals. For example, 10 months exposure to air
pollution decreased spatial learning in mice (Fonken et al., 2011), as
well as noise exposure for 15 days produces working and recognition memory decits in rats (Haider et al., 2012). The hippocampus
is known as the key region critically involved in both, spatial learning and memory formation (Broadbent et al., 2004; Kahlmann et al.,
2005). Thus, the toxicological ndings from experiments in rodents,
which show that noise exposure causes changes in hippocampal
neurotransmitter signaling in rats (Cui et al., 2012), support the
ndings by Fonken et al. (2011) and Haider et al. (2012). Similarly, associations of both air pollution and noise with psychological
functions were also demonstrated in animal studies. For example,
male mice exposed to long-term PM2.5 exposure and rats exposed
to sub-chronic noise exposure were found to display depressivelike symptoms (Fonken et al., 2011; Naqvi et al., 2012). However,
the biological pathways of possible effects of noise on psychological function are not well established yet. Briey, animal studies
shown that noise provokes mild acute stress similar to that occur
in human (Arnsten and Goldman-Rakic, 1998). This stress evokes
the release of high levels of noradrenaline and dopamine in hypothalamus that in turn impairs the regulation of prefrontal cortex
that is responsible for cognitive abilities (Arnsten, 2009).
Some common problems were identied in the reviewed studies
and they hinder a full comparison of results of these studies.

necessary to conduct studies on air pollution and noise using the

same clinical and subclinical outcomes to be able to adequately
compare and tease apart the effect of either exposure.
Individual susceptibility
When investigating the effect of trafc proximity (indicator for
trafc noise as well as for trafc-related air pollution) or noise, it
is also important to take into account a rising prevalence of hearing impairment with age. In two out of 22 reviewed studies (Ranft
et al., 2009; Wellenius et al., 2012), an association of trafc-related
air pollution with decreased cognitive function was found only in
the subgroup of younger participants (74 years and 77 years,
respectively), but not in the older group. A decline in hearing in
older age may lead to a lower sensitivity to trafc noise, thereby
diluting the effect of noise in study populations with a large fraction
of elderly participants.
Longitudinal data on cognitive decline
Only few studies on progression of cognitive impairment and
its association with air pollution and ambient noise also limit the
strength of the existing evidence. In adults, long-term exposure to
air pollution and ambient noise may have a negative effect on cognitive function that will result in cognitive impairment additional
to normal cognitive aging. Only two studies (Chen and Schwartz,
2009; Weuve et al., 2012) performed a comparison of air pollutionrelated cognitive decline with normal aging-related decline. In the
study of Chen and Schwartz (2009), an increase in 10 ppb of annual
ozone was associated with the decline in cognitive functions that is
equivalent to 3.5 till 5.3 years normal-aging decline. Similarly, in the
study of Weuve et al. (2012), differences in rates of global cognitive
changes per 10 g/m3 of PM2.510 and PM2.5 exposures were found
similar to the difference in rates between women who were 12
years apart in age. There is an urgent need for studies investigating the association of environmental exposures with progression
of cognitive decline in older age.
Additional covariates

Only one of the reviewed studies analyzed both air pollution

and noise association (Persson et al., 2007). However, even though
information on both exposures was available, no analysis with air
pollution and noise simultaneously was conducted, possibly due to
high correlation of these two exposures. Air pollution and ambient noise are both related to trafc and often occur simultaneously
in time and space. The effect of air pollution may be modied by
noise, and a synergism between the two exposures seems possible. It is therefore necessary to include both air pollution and noise
exposure into account when investigating the effect of either.

Most studies investigating air pollution or noise associations

took personal characteristics and life-style factors as potential
confounders into account. However, depressive symptoms, satisfaction with health and activities of daily living might play
an important role in cognitive performance. The effect of these
covariates is poorly investigated both in air pollution and noise
studies.
Similarly, the role of comorbidities is poorly investigated in the
current body of evidence. Five of reviewed studies (Brink, 2011;
Chen and Schwartz, 2009; Loop et al., 2013; Lim et al., 2012; Ranft
et al., 2009) included factors related to CVD (BMI, hypertension,
triglyceride level) as intermediates in sensitivity analyses, showing
an attenuation of effect in some studies. These are important analyses as they suggest that general or cardiovascular health may be
one clinical pathway through which a possible effect of air pollution
and noise can be mediated.

Diversity of outcomes

Role of gender in studies of neurocognitive functions

Studies related to cognitive and psychological effect of air pollution use different panels of tests than studies, which investigated
the effect of noise. Most of the studies exploring the effect of air pollution used a large battery of objective cognitive tests, while in noise
studies, investigators mostly used self-reported outcomes. Cognitive function was less investigated in noise studies, and completely
different tests were performed for its assessment. It is therefore

Five of the 22 reviewed studies were performed only in men or

women. Sex differences in different domains of cognitive function
have been described in several studies (Darley and Smith, 1995;
Meyers-Levy, 1989; Torres et al., 2006). However, few studies of
environmental exposures and cognitive function specically investigated potential effect modication by sex. For example, Gatto
et al. (2013) showed that logical memory was more affected by

Concurrent environmental exposures

10

L. Tzivian et al. / International Journal of Hygiene and Environmental Health 218 (2015) 111

long-term air pollution exposure in women than in men. In mouse

models, sex differences in behavioral patterns and neuron differentiation due to exposure to nano-sized particulate matter were
found (Davis et al., 2013). The role of sex in modifying effect estimates is largely unclear but may provide some insights into possible
biological mechanisms. Investigations of mixed gender populations
and stratication of results by sex are therefore necessary.
A lack of information on the length of residential exposure
Although the reviewed studies assessed long-term exposure to
air pollution and noise, length of residence at the same residential
address is not mentioned in most of these studies. Information on
years of living at the same address, and stratication of analysis
for participants that did or did not change the living address during
the whole period of exposure can help to provide the more accurate
estimates for the relevant exposureoutcome associations.
Conclusions
Investigations on the association of air pollution and noise mental health received increased attention during recent years. Both
exposures reviewed in this article (air pollution and noise) were
shown to be associated with one or several indicators of neurocognitive function, mood disorders and neurodegenerative disease
in several studies. Despite some limitations and inconsistencies
of reviewed studies, they generally support the hypothesis that
ambient air pollution and noise are associated with neurocognitive functions, mood disorders and neurodegenerative disease in
long-term exposed persons. Nevertheless, there is a need for studies investigating simultaneously air pollution and noise exposures
in association with mental health, for longitudinal studies to corroborate ndings from cross-sectional analyses, and for parallel
toxicological and epidemiological studies to elucidate mechanisms
and pathways of action.
Acknowledgements
Lilian Tzivian gratefully acknowledges the support by a postdoctoral fellowship from the Environmental and Health Fund,
Jerusalem, Israel. This work was supported by the German Research
Foundation (DFG; HO 3314/2-1).
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